Staph Aureus Flashcards
Characteristics of S. aureus
G+ cocci, facultative anaerobe
Cat+, salt tolerant
Coagulase+
b-hemolytic
Where is S. aureus found?
Flora of skin and mucous membranes
Cell wall of S. aureus
Capsule with many serotypes, protects from phagocytosis and helps adhesion (PGs, teichoic acid)
Peptidoglycan: more rigid cell wall, endotoxin-like (stimulates complement, IL-1, abscess formation)
Teichoic acid, protein A and coagulase
TA: phosphate polymers attached to PG helps attach to fibronectin
PR: FcR of IgG binds IgG before it can bind S. aureus
Coag: clumping factor, binds fibrinogen -> fibrin to build a protein wall and impede immune system/Abs
Virulence factors of S. aureus
*Not all produced by all S. aureus
Protein A, coagulase, elastin BP, collagen BP, fibronectin BP, clumping factor, enterotoxin B, TSST-1, alpha toxin, etc.
Toxins in S. aureus
5 cytolytic/membrane damaging, 2 exfoliative (SSSS), 8 enterotoxins (superAg, food poisoning), TSST-1 superAg
Alpha toxin source and effects
On bacterial chromosomes and plasmids
Causes pores in cell membrane, alters ion balance -> swelling, lysis
SSSS (Ritters Disease)
Surface staph infxn of neonates/young children produces A and B exfoliative toxins (serine proteases) to break desmosomes = blisters, sloughing off
*No bacteria in blister fluid b/c toxin-mediated
Bullous impetigo
Localized form of SSSS, specific S. aureus strains
Blisters are culture +
In children, highly communicable
Enterotoxins (food poisoning)
Stable to heat and GI enzymes; superAgs
Rapid (4h) vom/dia for 24 h w/o fever
In salted meats, custards, ice cream, potato salad - won’t taste spoiled
Toxic shock syndrome toxin (TSST-1)
Heat and protease resistant (chromosomal source)
SuperAg, penetrates mucosal barriers to cause systemic effects
Mechanism of superantigen & example
Bacterial toxin + MHC-2 and APC = non-specific activation T cells -> massive cytokine release (IL-1,2, TNF-a) -> n/v, fever, malaise -> shock, multiple organ failure, death
*S. aureus & Strep. pyogenes
Clinical manifestations of TSST-1
6000/year in US; localized growth followed by release of toxin into blood -> acute fever, hypotension, macular erythematous rash; can be fatal (5%) & high recurrence if AB ineffective
Infected tampon, wounds, surgery, burns
S. aureus diseases
SSSS, bullous impetigo, food poisoning, TSS, pyogenic cutaneous infections (impetigo, folliculitis, carb/furuncles), bacteremia, acute endocarditis, pneumonia/ empyema, osteomyelitis, septic arthritis
S. epidermidis & saprophyticus diseases
SE: endocarditis (native and prosthetic heart valves), catheter/shunt infections, prosthetic jj infxn
SS: UTI in young women
Epidemiology of staph
Ubiquitous, normal flora for many, shedding from skin is most common cause of nosocomial infxn, spread easily (*asepsis)
How did MRSA develop?
Picked up MEC-A (mobile gen element, chr cassette) gene through transposition -> modified PBP
Lab dx of S. aureus
Grows selectively on 6.5% NaCL agar + mannitol, coagulase+
Treatment, prevention, and control of staph
Pen-resistance on plasmid & other resistances common
Vancomycin usually works, but resistance increasing
Aminoglycoside resistance growing
Infection control of staph
Hygienic practices, hand washing, tracking by hospitals
